Evidence map›Paper›PMID 32064266›Full record

ReviewFrontiers in medicine2020

Bile Acid Receptor Therapeutics Effects on Chronic Liver Diseases.

Vik Meadows, Lindsey Kennedy, Debjyoti Kundu, Gianfranco Alpini, Heather Francis

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Unravelling the therapeutic landscape of bile acid-based therapies in gastrointestinal disorders.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association · 2024
    Review
  4. Article
  5. The Role of Inflammation in Cholestatic Liver Injury.Journal of inflammation research · 2023
    Review
  6. Bile Acid Regulates the Colonization and Dissemination ofJournal of fungi (Basel, Switzerland) · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Aberrant FGFR4 signaling worsens nonalcoholic steatohepatitis in FGF21KO mice.International journal of biological sciences · 2021
    Article
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Vik MeadowsRichard L. Roudebush VA Medical Center, Indiana University School of Medicine, Indianapolis, IN, United States.
Lindsey KennedyDivision of Gastroenterology and Hepatology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, United States.
Debjyoti KunduDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, United States.
Gianfranco AlpiniRichard L. Roudebush VA Medical Center, Indiana University School of Medicine, Indianapolis, IN, United States.
Heather FrancisRichard L. Roudebush VA Medical Center, Indiana University School of Medicine, Indianapolis, IN, United States.
Indiana University – Purdue University Indianapolis · USRichard L. Roudebush VA Medical Center · USIndiana University School of Medicine

Funding

The Paracrine Regulation of Mast Cells During Biliary/Cholangiocyte Repair and DamageR01DK108959 · NIDDK · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI FRANCIS, HEATHER L · 2016 to 2024
$2.5M
Mechanisms of mast cell/cholangiocyte regulation of non-alcoholic fatty liver disease progressionR01DK119421 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI FRANCIS, HEATHER L · 2019 to 2022
$1.4M
REGULATION OF CELLULAR SENESCENCE BY NON-CODING RNAS IN ALCOHOLIC LIVER INJURYR21AA025997 · NIAAA · SCOTT AND WHITE MEMORIAL HOSPITAL · PI ALPINI, GIANFRANCO D, MENG, FANYIN · 2017 to 2018
$435k
Mechanisms of synergistic regulation of biliary inflammation and fibrosisI01BX003031 · VA · RLR VA MEDICAL CENTER · PI FRANCIS, HEATHER L · 2016 to 2023
–
BLR&D Research Career Scientist AwardIK6BX005226 · VA · RLR VA MEDICAL CENTER · PI FRANCIS, HEATHER L · 2020 to 2024
–
BLRD VA I01 BX000574BLRD VA I01 BX003031BLRD VA IK6 BX004601BLRD VA IK6 BX005226NIAAA NIH HHS R21 AA025997NIDDK NIH HHS R01 DK108959NIDDK NIH HHS R01 DK119421
6 · The paper itself

Abstract

In the past ten years, our understanding of the importance of bile acids has expanded from fat absorption and glucose/lipid/energy homeostasis into potential therapeutic targets for amelioration of chronic cholestatic liver diseases. The discovery of important bile acid signaling mechanisms, as well as their role in metabolism, has increased the interest in bile acid/bile acid receptor research development. Bile acid levels and speciation are dysregulated during liver injury/damage resulting in cytotoxicity, inflammation, and fibrosis. An increasing focus to target bile acid receptors, responsible for bile acid synthesis and circulation, such as Farnesoid X receptor and apical sodium-dependent bile acid transporter to reduce bile acid synthesis have resulted in clinical trials for treatment of previously untreatable chronic liver diseases such as non-alcoholic steatohepatitis and primary sclerosing cholangitis. This review focuses on current bile acid receptor mediators and their effects on parenchymal and non-parenchymal cells. Attention will also be brought to the gut/liver axis during chronic liver damage and its treatment with bile acid receptor modulators. Overall, these studies lend evidence to the importance of bile acids and their receptors on liver disease establishment and progression.

Indexed as

bile acidbile acid receptorchronic liver diseaseobeticholic acidursodeoxycholic acid

Identifiers

PMID32064266
PMCPMC7000431
OpenAlexW3003796365

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.